Blood pressure sensitivity to sodium intake is present in 50 to 60% of patients with hypertension. 1 , 2 Epidemiologic studies suggest that there is a variety of pathophysiologic mechanisms leading to sodium-sensitive hypertension. For example, when sodium sensitivity of blood pressure has been evaluated in large numbers of hypertensive patients, a unimodal distribution is observed. 3 Second, on theoretical grounds, a number of differing pathophysiologic mechanisms have been described, including low renin essential hypertension, bilateral renal parenchymal damage, and nonmodulating essential hypertension. 4 – 6 Even in these broad subgroups, heterogeneity of mechanisms likely exists, i.e., low renin levels can occur in older subjects, probably reflecting vascular damage within the kidney, or in patients with diabetes, secondary to the metabolic derangements. Contrarily, some subjects with low renin hypertension demonstrate an enhanced adrenal response to angiotensin II. 7 – 9 In these subjects, the sodium sensitivity of the blood pressure is produced by mechanisms presumably analogous to those present in patients with primary aldosteronism.